Anderson, Louise A. MS, RN
"I feel like I have a time bomb ticking in me" is a comment frequently used by individuals to describe their feelings about having an abdominal aortic aneurysm (AAA). This sentiment also accurately reflects the concerns of health care providers who treat this condition. AAA is a chronic, progressive disease that is often asymptomatic and frequently evolves into rupture and death.1 The goal of managing an AAA is elective surgical repair, restoring aortic lumen integrity and preventing fatal blood loss and ischemia to vital organs. The incidence of AAA is increasing,2 and it currently ranks as the 13th leading cause of death in the United States, making it a vascular condition that nurses will encounter frequently. Nurses require in-depth knowledge about AAA to maximize patient survival and recovery. This article provides that knowledge by defining AAA and reviewing its pathogenesis, incidence, natural history, and clinical manifestations. In addition, the article describes the surgical and post-operative management of this condition and associated nursing care.
DEFINITION AND PATHOGENESIS
The most widely accepted definition of AAA is that it is a permanent localized dilation of the aorta that is at least 50% larger than the normal or expected diameter.2 An adjacent normal artery segment is used to determine the difference in size. Although aneurysms occur at different sites of the aorta as well as in other large arteries, the infrarenal aorta is the most common site of AAA with a frequency of 65%.3 Fig 1 illustrates other sites of aneurysms and their frequencies.2-4
Historically, the most frequent cause of aortic aneurysm was atherosclerotic changes in the vessel wall.5 However, over the last 20 years, this widely accepted theory has been challenged by a substantial body of evidence that proposes that atherosclerosis is only part of the pathogenic picture. Emerging theories propose that AAA development involves several factors that decrease the integrity of the basic structure of the aorta. Aneurysms are no longer considered atherosclerotic in etiology. They are now termed degenerative or nonspecific. Degenerative disease accounts for more than 90% of all infrarenal AAA.5
The fundamental histopathologic change in the aneurysmal aortic wall is the degeneration of the arterial media with complete disruption of the normal vessel architecture.6 The media consists of closely packed layers of smooth muscle cells in close association with elastin and collagen. Elastin provides elasticity to the vessel, allowing it to double its diameter with pressure increases and to recoil to its original dimensions with pressure decreases. In contrast, collagen is responsible for mechanical strength and limits the amount of distention and prevents disruption.7 Elastin content is greatest in the thoracic aortic and least in the distal portion, which, interestingly, is the most common location of AAA.6 There is no evidence that elastin is synthesized in adult life and has a half-life of 40 to 70 years.8 Therefore, it may lose its properties over time, explaining why AAA occurs primarily in people over 50 years of age.
In AAA, the media thins and only fragments of smooth muscle cells, collagen, and elastin fibers remain.9 The percentage of elastin in normal aortic tissue is 36% compared with 8% found in aneurysmal tissue. Similarly, lower amounts of collagen were found in the media of aortas in some individuals with an AAA. Reasons for these changes may be due to abnormal proteolytic enzyme activity affecting elastin and collagen synthesis and degradation.8-10 It is hypothesized that the normal proteolytic activity of elastase and collagenase causes increased synthesis and degradation of elastin and collagen, as well as a loss of inhibitory control.
Other pathogenic theories focus on the roles of trace metals and an inflammatory response in the media and adventitia.11 Abnormalities in trace metals such as copper and zinc are thought to be related because they are necessary for the maturation of collagen and elastin. However, research evaluating their role is inconclusive about their importance. The inflammatory theory has more merit as having a central role in AAA development.5 Whether a specific pathogen or an immune response to a pathogen causes the inflammatory reaction is not understood.5
Theories of genetic predisposition for AAA began with anecdotal reports of familial clustering, reported in the late 1970s.12 These early observations were later confirmed by larger surveys conducted on families with AAA.13-14 Results demonstrated that first-degree relatives who were male siblings of the relative with the AAA were at greater risk of having an AAA than female siblings. Furthermore, if the individual with the AAA is female, there is a greater chance that her relatives will be affected. The expected prevalence of AAA in the general population over 50 year of age is accepted to be between 2% and 4%. In comparison, the reported prevalence of AAA in affected families is reported to be 15% to 33%.
The natural history of AAA is difficult to determine. Some authors assert that AAA will continue to expand with eventual rupture unless death occurs from another cause.15 Different patterns of expansion have been observed in patients with AAA who have been followed by serial noninvasive methods. Some aneurysms may remain stable for long periods while others progressively enlarge. Still others may have rapid expansion.15 The average expansion rate has been estimated to be a 10% increase in diameter per year.16 Despite the available information on aneurysm growth patterns, the rate of growth for an individual is unpredictable.5
The single factor that consistently correlates with aneurysm rupture is its size, which is described by diameter and length.2 The diameter is the important dimension used to determine risk of rupture.5 The predicted rupture risk based on the aneurysm diameter is as follows: less than 4 cm, 0% per year; 4 to 5 cm, 0.5% to 5% per year; 5 to 6 cm, 3% to 15 per year; 6 to 7 cm, 10% to 20% per year; 7 to 8 cm, 20% to 40% per year; and more than 8 cm, 30% to 50% per year.5
Other risk factors identified with rupture are an abnormally elevated diastolic blood pressure and chronic obstructive pulmonary disease (COPD).5 The association between hypertension and aneurysm rupture is based on Laplace's law, which states that tension on the wall of a sphere is directly proportional to the radius of its lumen and the pressure exerted from within. Hence, the higher the diastolic pressure, the greater the likelihood of rupture. In the case of COPD, it is speculated that the increased proteolytic activity present in pulmonary connective tissue also may adversely alter aortic connective tissue, promoting rupture. Although the relationship between smoking and COPD is well established, an independent risk between smoking and rupture has not been demonstrated.5
CLINICAL MANIFESTATIONS AND DIAGNOSIS
AAA occurs most frequently in elderly white males with the onset occurring around age 50 for men and age 60 for women.17 The incidence steadily increases with age, reaching a peak around 80 years of age.17 AAA is five times more common in men than women and is more frequent in smokers and people with hypertension, coronary artery disease (CAD), COPD, or hyperlipidemia.18 As noted previously, familial clustering also is associated with increased prevalence.
The clinical manifestations of AAA differ according to the three categories of clinical presentation (ie, asymptomatic, symptomatic, and rupture). Approximately 66% to 75% of AAAs are asymptomatic.5 These asymptomatic AAAs can be diagnosed during a routine physical examination by palpation of a pulsatile abdominal mass located at or slightly above the umbilicus in the epigastrium. Detection by palpation is easier in a thin patient. However, patients who are thin, hyperdynamic, or have a tortuous aorta may have a prominent nonaneurysmal pulse that can be mistaken for an AAA.5 Palpation of AAA in obese patients is less accurate; when an AAA is found in these patients, they are generally large. An AAA should be suspected when peripheral aneurysms are found because at least one third of patients with a femoral or popliteal aneurysm also will have an AAA.5 Incidental diagnosis of asymptomatic AAA is often made during radiographic studies prescribed for a seemingly unrelated condition. For example, an AAA may be seen on computerized tomography (CT) scan prescribed for abdominal or spinal complaints.
In symptomatic AAA, patients frequently report vague abdominal pain, usually located in the epigastrium, that may radiate to the back, flank, or groin.15 This pain, which may intensify, is believed to be caused by rapid expansion of the aneurysm that stretches the overlying peritoneum.15 Symptoms in a patient with a known AAA require urgent evaluation to rule out rupture. Other symptoms of an AAA result from compression of the aneurysm on adjacent structures, distal embolization from thrombus within the aneurysm, and aortic occlusion due to thrombosis of the aneurysm.2 Table 1 lists these symptoms and their causes.
Rupture is the most lethal clinical presentation of AAA. The triad of symptoms associated with a ruptured AAA are a sudden onset of severe abdominal pain, hypotension, and the presence of a pulsatile mass.15 Abdominal pain occurs most frequently, is constant, and is not altered by a change in position. If bleeding occurs in the retroperitoneum, pain may radiate to the groin and scrotum as a result of compression and irritation of retroperitoneal tissue and sciatic nerve roots.15 If the aneurysm ruptures directly into the peritoneal cavity, rapid, massive hemorrhage occurs followed by cardiovascular collapse and death. Survival is favored when a small leak is contained from either tamponade from surrounding structures or clot at the site of the leak. Most of these patients present with transient hypotension that develops into shock over the next several hours.15 A contained rupture can provide enough time to get the patient to an emergency center. The stability of the patient dictates the amount of time available for diagnostic imaging. Because of the high mortality associated with a ruptured AAA, its diagnosis should be considered in any elderly patient with abdominal or flank pain.
Ultrasonography (US) is the preferred method for initial evaluation of a suspected AAA. Improved technology with refined resolution of anatomic detail provides accuracy in size measurement to within 5 mm.19 It is noninvasive, readily available at most hospitals, and a cost-effective choice for initial and serial AAA surveillance. However, US does not provide information about the adjacent vascular anatomy and structures, which is necessary for operative planning. In addition, US is not able to determine the presence of rupture.5 Also, obesity and intestinal gas can interfere with visualization of the aorta and iliac vessels in US. More detailed images can be obtained from the following tests: contrast enhanced CT scan, angiography, magnetic resonance imaging (MRI), or magnetic resonance angiography (MRA).
CT scans are the best study for preoperative assessment of AAA.5 They give accurate measurements to within 5 mm19 and define the relationship of the aneurysm to the surrounding anatomy (see Fig 2). Determining the relationship of the AAA to the renal arteries and defining major venous and renal anomalies and other pathologic findings are important for planning the surgical approach. Newer advances in three-dimensional and sagittal CT reconstruction provide even more detailed images with excellent resolution.5 Like US, CT scans are readily available but have the disadvantages of contrast agent exposure and increased expense.
Although angiography provides an excellent picture of the adjacent vascular anatomy, it is not a good test for diagnosing or sizing an aneurysm.15 The presence of intraluminal thrombus limits the distribution of the contrast, which can lead to underestimation of size. Although some surgeons still prefer to use angiography routinely, the absolute indications for that procedure are to evaluate concurrent vascular disease suggested from signs and symptoms of arterial occlusive disease involving the renal, mesenteric, or lower extremity vasculature.5
Studies comparing the results of MRA with CT scans and angiography have found MRAs to be highly accurate. Unfortunately this technology is expensive, has limited availability, and excludes patients with metallic devices or who have claustrophobia. These disadvantages do not make it the test of choice for preoperative evaluation.5
PREOPERATIVE ASSESSMENT AND MANAGEMENT
Patients are considered for elective repair of the AAA when the risk of rupture becomes greater than the risk of surgery.5 These factors must be evaluated in relation to the individual's life expectancy and concurrent morbidity. Most authorities recommend surgery for AAAs that are 5 cm or greater in a person with a reasonable life expectancy and low or modifiable risk factors.5 For symptomatic or rapidly expanding aneurysms, regardless of size, the decision to operate is more straightforward, and surgery is recommended.5
Current series report that elective repair can be done successfully with a 2% to 5% mortality rate.20 Urgent repair of intact symptomatic AAA has approximately an 18% mortality rate with lack of time for a careful evaluation of concurrent medical problems being cited as the primary cause for the higher death rate.15 Unfortunately, the mortality rate when rupture occurs is much higher, approaching or exceeding 50% in the patients who reach the hospital.21
CAD is the most serious concurrent medical condition affecting operative risk of the AAA patient, and myocardial infarction is a major cause of perioperative mortality. In order to decrease the risks of dying from CAD, preoperative detection should be completed. Although there are varying opinions on the best way to do this, there is agreement that using cardiac symptom severity in combination with noninvasive cardiac stress testing can provide adequate information to determine the patient's level of risk and need for coronary angiography.5 It is recommended that patients who have angiographically proven CAD have a myocardial revascularization procedure prior to AAA repair.
Perioperative management of myocardial ischemia can be accomplished by the administration of beta-adrenergic blockers, which decrease the workload of the left ventricle. Vascular surgery patients who received intravenous metoprolol demonstrated less intraoperative ischemia than untreated controls.22 In addition, mortality due to cardiac causes was reduced for up to 2 years in general surgery patients at risk for CAD who received atenolol.23 Based on these findings and additional data that showed reduced aneurysm expansion with beta blockade,24 these drugs are recommended for AAA patients in the preoperative and postoperative period. Maintaining a hematocrit level of 28% to optimize oxygen delivery also can prevent myocardial ischemia.25
Other conditions that increase the risk of elective repair are the presence of other cardiac diseases such as dysrhythmias and congestive heart failure, decreased renal function, atherosclerotic disease in other peripheral vessels, hypertension, hyperlipidemia, COPD, smoking, morbid obesity, liver disease, and diffuse retroperitoneal fibrosis.15 Although age over 80 years is included as a factor increasing the operative risk, the physiologic age of individuals is more important than the chronologic age.15 As in the case of managing CAD, optimizing preoperative treatment of concurrent medical conditions and risk factor reduction should be included in the plan of care. Other preoperative tests that are standard for any major abdominal operation also should be included in the preoperative assessment.
Most patients receive general anesthesia for an AAA repair. Supplemental continuous epidural anesthesia is frequently used for its benefits of allowing a lighter level of general anesthesia as well as providing a delivery system for postoperative pain control. Intravenous antibiotics are administered preoperatively and for 24 hours after surgery to reduce the chance of prosthetic graft infection. Placement of a central venous catheter, arterial pressure monitoring catheter, nasogastric tube, and foley catheter is standard procedure prior to surgery. In high-risk cardiac patients, a pulmonary artery catheter may be placed to monitor cardiac function and fluid balance.5 Normal body temperature should be maintained during surgery to prevent coagulopathy, allow extubation, and maintain metabolic function.5
For elective AAA repair, a midline transperitoneal incision from the xyphoid to the symphysis pubis is the most widely used approach. First, the abdomen is explored for intraabdominal pathology such as cancer. Next, the transverse colon is retracted superiorly, the small bowel is placed to the right, and the peritoneal incision is made to expose the AAA. The proximal aorta is dissected first, followed by dissection and control of the iliac arteries. The quality of the renal, superior, and inferior mesenteric arteries is assessed by careful palpation.5
Once the aorta has been exposed, a prosthetic graft of appropriate size is chosen from knitted Dacron, knitted Dacron impregnated with collagen or gelatin, woven Dacron, or polytetrafluoroethylene (PTFE). The last three choices, which are the most popular, do not require preclotting to prevent leaking and save time. In addition, these grafts allow more accurate sizing of graft to aorta because graft selection can be delayed until the aneurysm is opened. It should be noted that the superiority of one graft over another has not been established in controlled trials.5
Prior to aortic cross-clamping the patient is anticoagulated with heparin to reduce lower extremity thrombotic problems. Distal clamps are applied first to prevent distal embolization from calcific atherosclerotic plaque followed by proximal clamp placement. The aneurysm is opened lengthwise along its anterior surface, and a horizontal incision is made below the neck of the aneurysm.5
It is common to have intraluminal thrombus and atherosclerotic debris present in the aneurysm sac. This is removed, and control of collateral flow into the sac is obtained. If the aneurysm does not involve the iliac arteries, a tube graft is used with the proximal aortic anastomosis completed first followed by the distal anastomosis at the aortic bifurcation. If the iliac arteries are aneurysmal, then a bifurcated graft or inverted-Y-shaped graft is used. After the first iliac anastomosis is completed, the limb of the graft is unclamped, restoring flow to that extremity. The contralateral side is managed in the same way. It is important that the unclamping be done slowly to avoid hypotension that can occur with filling of the dilated distal bed.5
Next, the colon is evaluated for ischemia. Also, lower extremity perfusion equal to baseline assessments and the absence of signs of distal embolization should be confirmed. A change in perfusion status indicates the need for a thrombectomy. Last, the aneurysmal sac is trimmed and sutured to cover the graft, providing a natural tissue barrier over the prosthesis. The retroperitoneum is closed, the small bowel is inspected and returned to its anatomic position, and the wound is closed according to the surgeon's preference.5
An alternative method for repairing AAA is the retroperitoneal approach, which uses a flank incision and requires less intestinal exposure and manipulation. Research5 suggests that this exposure promotes quicker return of gastrointestinal function, reduces postoperative pulmonary complications, is less painful, and reduces length of stay when compared with the abdominal approach. However, this finding has not been substantiated by additional studies. This approach is preferred for patients with significant cardiac or respiratory compromise, an abdominal wall stoma, or the presence of multiple abdominal adhesions.5
IMMEDIATE POSTOPERATIVE CARE
In order for the nurse to perform appropriate patient assessment, anticipate and identify needs or problems, and provide expert care, knowledge of complications specific to the surgical repair and the patient's concurrent medical problems is essential. Currently, patients who have an elective open repair of their AAA will go to the surgical intensive care unit. The length of stay varies depending on their cardiorespiratory and hemodynamic stability. A recent study26 evaluating "fast tracking" of aortic reconstructive patients by using early extubation protocols reported that the majority of patients can be safely extubated in the early postoperative period. If early extubation becomes standard care, it will have a great impact on the intensive care length of stay.
Cardiac and hemodynamic complications
It already has been noted that the high incidence of CAD is strongly associated with a major cause of perioperative mortality, myocardial infarction. Other cardiac dysfunctions such as dysrhythmias and congestive heart failure also are observed. Optimization of cardiac function during the perioperative period through inotropic support, afterload reduction, adequate oxygenation, blood pressure control, appropriate volume management with the hematocrit maintained at 28%, and short aortic clamp times reduces the risk of myocardial stress.5 The major goals of the nurse are to assess cardiac function and systemic perfusion and minimize the workload of the heart.
Besides the preexisting CAD, other factors that increase myocardial ischemia are the hemodynamic changes that occur with aortic cross-clamping and declamping.5 As the aorta is cross clamped cardiac afterload increases and hypertension occurs. There is a decrease in ventricular contractility, cardiac index, and coronary artery perfusion due to the rapid rise in left ventricular end-diastolic pressure. Distally, the lower extremities develop temporary ischemia followed by compensatory vasodilation. In contrast, declamping and the return of blood flow to the legs cause hypotension or aortic declamping shock. Sudden restoration of flow into the vasodilated distal circulation reduces afterload, while increased venous volume reduces preload. Furthermore, acidic metabolites and other ischemic vasoactive substances that mix with the systemic circulation create a metabolic acidosis that decreases vascular tone and myocardial function. Declamping shock can be minimized with volume replacement started prior to clamp release and by removing the clamps slowly to allow for gradual return of distal flow.5
Cardiovascular monitoring includes continuous telemetry and the continuation of the various levels of invasive monitoring initiated prior to surgery. The nurse will monitor cardiac function and hemodynamic status by obtaining pulmonary artery pressure, pulmonary artery wedge pressure, central venous pressure, cardiac output, and systemic vascular resistance as well as systemic arterial pressure.27 Postoperative serial electrocardiograms and cardiac enzymes may be done as indicated to assess for myocardial damage. In addition to monitoring these physiologic parameters, assessing the patient's pain level is an important nursing function. By assuring good pain control, cardiac complications can be decreased by reducing the catecholamine stress response.
If large amounts of fluid were required intraoperatively, the patient may gain excessive fluid weight that can aggravate third spacing. The resulting hemodilution decreases oxygen-carrying capacity and increases preload past a therapeutic level adding further myocardial stress. Precisely measuring intake and output, taking daily weights, assessing pulmonary and peripheral edema, and monitoring electrolyte and blood urea nitrogen and creatinine levels are necessary to assess the patient's fluid balance and return to homeostasis. This generally begins within 48 to 72 hours after surgery with a generalized diuresis accompanied by weight loss and a reduction in edema. The resolution of third spacing can be a critical time for patients who are usually increasing their activity during this resolution phase. Nurses need to know that the increased activity, in addition to the increase in intravascular volume from third spacing, causes more work for the heart. Therefore, the patient's cardiovascular tolerance of activity must be included in the daily assessment.
Renal failure after aneurysm repair can occur due to hypoperfusion of the kidney secondary to emboli, hypotension, and aortic cross-clamping.5 The effect of cross-clamping is more hazardous in the case of a suprarenal aneurysm.28 Renal vasoconstriction and intrarenal redistribution of blood flow that occurs during surgery also have been suggested as etiologies for renal dysfunction, but this theory is not well understood.29 Patients with preoperative renal insufficiency are at greater risk for postoperative renal failure.28
Renal failure resulting from emboli usually develops in the immediate postoperative period in comparison to acute tubular necrosis, which may not be apparent until several days later. The same strategies used to maximize cardiac function also are important in preserving renal function. In addition, some authorities recommend administering intraoperative mannitol or furosemide to promote adequate urine output and preserve renal function.5 Urine output should be over 30 mL per hour. The previously discussed nursing care involving the cardiac and hemodynamic assessments also will provide information for evaluation of the patient's renal function.
Arterial thrombosis and embolization from atherosclerotic debris or mural thrombus are other major causes of complications. Thrombosis may occur in a native vessel or in the limb of a bifurcated graft. In order to prevent thrombosis from low distal flow during cross-clamping, the patient is fully anticoagulated prior to clamp application. Frequent sites of embolization are to the distal arterial tree and the microcirculation.5 Embolization can be minimized by carefully applying vascular clamps, avoiding unnecessary manipulation and dissection, and performing flushing maneuvers prior to unclamping.5
Embolization or thrombosis, which threatens the viability of a limb, is usually found after distal blood flow is reestablished and poor perfusion and absent distal pulses are observed. This generally requires a thrombectomy to restore blood flow. Thrombosis of the microcirculation may not be evident until several hours after surgery when signs of cutaneous necrosis start to appear. Toes and feet are common areas affected, and the condition is sometimes referred to as "trash foot."29 Larger areas such as the thigh or buttocks also may be involved. The areas involved may first appear cyanotic or mottled and are usually painful. Depending on the extent of injury, tissue loss and gangrene may occur. One recommended treatment is early administration of low-molecular-weight dextran for several hours after the operation. Still the most frequent treatment is careful observation, supportive wound care, pain control, and waiting for demarcation of tissue loss to occur. In some cases amputation may be required.5
Evaluation of the patient's peripheral vascular status includes assessing for the 5 Ps of ischemia: pain, pallor, pulselessness, paralysis, and paresthesia. Bedside ankle brachial indexes can be done when indicated. The skin of the patient's lower body should be carefully inspected for signs of embolization and basic principles of pressure ulcer prevention should be applied.
The most serious gastrointestinal complication that can occur after an AAA repair is colon ischemia, which usually involves the sigmoid colon; it also is termed ischemic colitis.5 It can be due to concurrent occlusive disease or embolization to the major collaterals in the superior mesenteric or hypogastric circulations. Decreased cardiac output and colonic distention also may be causative factors. Ischemic colitis should be suspected if the patient requires excessive fluid replacement in the first 8 to 12 hours after surgery. Additional signs are bloody diarrhea, abdominal distention, leukocytosis, fever, and acidosis.5 In order to confirm the diagnosis and determine the extent of colon involvement, a colonoscopy must be performed. In most cases the necrosis is limited to the mucosa and resolves spontaneously without additional surgery. When there is full-thickness colonic necrosis, prompt surgical intervention is required to limit contamination of the peritoneal cavity and the vascular graft. Resection of the necrotic colon with descending colostomy is usually required.5
Paralytic ileus, the common gastrointestinal dysfunction that occurs after any major abdominal procedure, may be more prolonged after aneurysm resection. This is due to the evisceration and dissection at the base of the mesentery that is required in the repair.5 Careful monitoring of the patient's intake and output and return of bowel function during the entire hospital stay is important.
There are several other complications associated with AAA surgery. Hemorrhage, a risk of any operation, usually results from problems with the proximal aortic anastomosis or an iatrogenic venous injury.5 Respiratory problems may occur more frequently because of the increased prevalence of AAA in smokers and patients with COPD. Injury to the ureters and bowel, which can cause devastating consequences related to infection, is seen most frequently in emergent repairs, cases with extensive fibrosis, or where the structures are anomalous to their usual position.29 Early graft infection is rare and often is associated with bowel injury, but it also occurs frequently with femoral artery graft placement.5 Despite the rarity of graft infection, it is recommended that patients receive antibiotic prophylaxis during high-risk procedures such as dental care and endoscopy procedures for a minimum of 6 months after the AAA repair. Last, paraplegia due to spinal cord ischemia occurs rarely and is a complication more often associated with a thoracoabdominal aneurysm.30
LATE COMPLICATIONS AND LONG-TERM FOLLOW-UP
As in other surgeries, length of stay for an AAA patient has steadily declined. Benchmark data recommend a 4- to 5-day hospital stay for an uncomplicated recovery.31 However, care of the patient does not stop at discharge. After the initial postoperative visits done to ensure recovery from a major surgical procedure, these patients should be seen every 1 to 2 years to monitor for late complications that occur in approximately 7% of patients.32 These complications include aneurysmal disease in other major vessels, pseudoaneurysms at the graft anastomosis, graft infection, aortoenteric fistula, and, in the case of bifurcated grafts, graft limb occlusion.5 All these complications require surgical intervention and are associated with significant morbidity and mortality.
Sexual dysfunction may not be reported until later follow-up visits. Injury of autonomic nerves during para-aortic dissection, particularly along the left side of the infrarenal aorta, can cause impotence or retrograde ejaculation.33 Other causes of impotence should be considered, and patients should be counseled about corrective therapies.
Long-term follow-up also provides an opportunity for patient education on potential complications, risk factor modification, especially with regard to hypertension and smoking, and the need to screen the patient's high-risk family members for aneurysmal disease.
Vascular surgeons, like other areas of surgery using minimally invasive techniques, are evaluating the use of endovascular grafts to repair AAA. The procedure can be done under local or general anesthesia and requires a team approach including a surgeon, an interventional radiologist, and nurses trained in the procedure.34 The graft, which is contained in a deployment catheter device, is inserted through the femoral artery via a groin incision, advanced across the aneurysm, deployed, and anchored in a nonaneurysmal healthy vessel. Self-expanding or balloon-expanding stents with anchoring devices are used to fix the graft to the vessel wall. In this way the proximal and distal aneurysmal vessel is completely excluded or sealed off from the general circulation. Over time, the aneurysm sac undergoes a reduction in size and volume.35 Proper positioning of the graft is of major importance and is confirmed by fluoroscopy with radiographic contrast or intravascular ultrasound.34
Endovascular repair has several advantages. From a procedural perspective, it avoids the risks associated with a laparotomy, cross-clamping the aorta, and blood loss that occurs when an AAA is incised.35 From the patient's point of view, the endovascular technique means a smaller incision with less pain; minimal alteration in cardiac, pulmonary, and gastrointestinal function; a shorter hospital stay; and a quicker return to baseline lifestyle.36 However, not all aneurysms are anatomically appropriate for endovascular repair. Not being a suitable candidate is a major disappointment for the patient, who must be addressed with empathy as well as explanation.36
These advantages affect the acuity level of the patient, which is lower when compared with the patient who has an open repair. Less nursing care is required for intensive care monitoring, pain medication administration, patient mobility issues, and return to baseline function.36 The usual hospital length of stay is 1 to 2 days. However, this decreased acuity does not mean a decrease in potential complications that can occur during or after the procedure. Table 2 lists local and vascular complications associated with endovascular AAA repair. Problems caused by hemorrhage from injury to access vessels, embolization, and wound complications have been discussed in the section on open AAA repair and are not covered further here. The remaining complications are unique to the endovascular procedure, and nurses need to be aware of them in order to provide comprehensive care.
Endoleak is defined by the persistence of blood flow outside the lumen of the endoluminal graft but within the aneurysm sac or adjacent vessel also involved in the procedure.35 A type 1 endoleak develops when the graft fails to exclude the blood flow at the proximal, mid-graft, or distal graft anchor sites. In a type 2 endoleak the graft seal is usually complete, but there is blood flow into the aneurysm sac from collateral blood vessels. Persistent endoleaks allow for continued aneurysm expansion and risk of rupture.35 Endoleaks may be managed by observation, further endovascular procedures, or conversion to an open repair. They are usually asymptomatic and are diagnosed by serial CT scans obtained within 1 week; 6, 12, and 18 months; and then annually. The majority of vascular surgeons manage endoleaks by observation since they can seal spontaneously. The persistence or reoccurrence of the endoleak as well as the risk of AAA rupture dictates when another intervention is indicated.35
Post-implant syndrome can occur immediately after graft implantation and may last up to 7 days. The cause is unknown and is usually associated with thrombosis within the aneurysm sac.35 The patient will have back pain and fever without a leukocytosis or other signs of infection. Treatment is based on symptom management; nursing care should include an assessment for other sources of infection. Special attention should be given to the groin incisions since these areas are frequently involved with minor wound complications such as infection, lymphoceles, and hematomas.37
Graft limb thrombosis
The causes of thrombosis in an endovascular repair are more dependent on the procedure and changes that evolve in the aneurysm after the procedure than the thrombosis that occurs in open repairs. Arterial dissection that can occur during the passage of the catheter and kinking of the graft in the iliac arteries are the most common causes of thrombosis related to technique.35 In the case of post-procedure changes in the aneurysm, the thrombosis occurs when the aneurysm decreases in size and previously straight limbs of the graft may kink and form endoluminal clots.35 The signs and symptoms and required nursing care with an endovascular graft limb thrombosis are the same as in an open AAA repair.
Currently there are several endovascular grafts that are being researched and refined in Europe and the United States. Initial results suggest that the procedure is safe and is an appropriate method for AAA repair.35 Additional research with long-term outcome data on the durability of the grafts and their ability to arrest the natural history of aneurysms is required to establish if this technique will be the future method of choice for the majority of patients with an AAA.
Over the last several decades, knowledge about AAA has steadily increased, improving the treatment and patient outcomes. New theories have emerged about the pathogenesis of AAA and its risk for rupture. More precise radiographic imaging is available for diagnosis, and improved perioperative cardiovascular and anesthesia management have decreased the associated morbidity and mortality. Most recently, the increasing experience with endovascular treatment has the potential for dramatically changing the standard of care for AAA. Nurses must incorporate this new information as well as established principles of patient management into their nursing care in order to meet the challenges of the AAA patient.
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